T-lymphocytes are involved in the pathogenesis of many diseases. They comprise an intrinsic part of the immune response to infectious agents, may play a role in host defense to malignancies and represent the major target of human lymphotropic retroviruses, including HIV. They have been implicated in the immunologic autoresponsiveness seen in a variety of inflammatory disorders of uncertain etiology. Autoreactive T-cells have been hypothesized to be critical in rheumatoid, arthritis, the early onset form of insulin dependent diabetes mellitus, multiple sclerosis and a number of other illnesses. Observations made in animal models of these diseases have indicated that a restricted population of t-lymphocytes, or defined antigenic specificity, is present and that therapeutic approaches directed at exploiting the homogeneity of the responding elements should be useful. It has been suggested that the observations made in the animal models, indicating restricted T-cell receptor use, also prevail in the homologous human diseases. The proposed meeting brings together investigators from many countries, working in both human and animal systems, whose data bear on the question of the restricted nature of the T-cell receptors, their pathogenetic relevance, and the implications for therapy. In plenary sessions senior investigators will review the current status of t-cell repertoire selection and receptors usage in normal immune responses, comparing data from human and animal studies, and present data supporting either the oligo or polyclonal nature of autoimmune t-cell response in various clinical settings. Combined poster/workshop sessions focussed on specific diseases will allow younger investigators, in particular, to present their data in a more informal context. Issues of methodologic comparability and reproducibility of data will be discussed and hopefully resolved. Where inconsistency still exists, experimental approaches to reconciling conflicting data will be developed.